Dr. Siminovitch has a long-standing
interest in characterizing signaling pathways that regulate immune cell
function. Her lab played seminal roles in defining the functions of the
SHP-1 tyrosine phosphatase in autoimmune responses and the
Wiskott-Aldrich syndrome protein (WASp) actin regulator in immune
deficiency, and her group continues to generate new mouse models that
can be used to delineate the contributions of these and other tyrosine
phosphatases and cytoskeletal modulatory proteins to immune cell
function.

Dr. Siminovitch is also an acclaimed
leader in genomic medicine. Working with other physicians at the
Rebecca MacDonald Centre for Arthritis and Autoimmune Disease, Dr.
Siminovitch has discovered some of the key gene variants conferring
risk for rheumatoid arthritis and primary biliary
cirrhosis.

By coupling her studies of human
patient cohorts with the generation of unique mouse models, she is
characterizing the genes that regulate normal immune responses,
defining the mechanisms whereby certain proteins contribute to immune
system function, and identifying the molecular pathways whereby such
variants evoke cell dysfunction and disease. Dr. Siminovitch also
directs a core facility that provides genotyping and sequencing
services as well as guidance for design of genomics projects aimed at
delineating the genetic factors modulating disease risk and
outcome.

Aims to provide new knowledge that will lead to individualized
medicine

Major Research
Activities

Dr.
SiminovitchÂ´s research program is directed at identifying the genetic
and cellular mechanisms modulating expression of the immune response
and development of immunologic diseases. The lab is now focused on
defining the molecular events conferring risk for and modulating
outcome of chronic autoimmune inflammatory diseases and in particular
rheumatoid arthritis, primary biliary cirrhosis and Wegenerâ€™s
granulomatosis. To this end, the lab capitalizes on its access to
unique mouse models and patient cohorts to delineate the gene variants
conferring risk for these diseases and the effector pathways linking
such variants to disease.